Abstract
MYC is a target of the Wnt signalling pathway and governs numerous cellular and developmental programmes hijacked in cancers. The amplification of MYC is a frequently occurring genetic alteration in cancer genomes, and this transcription factor is implicated in metabolic reprogramming, cell death, and angiogenesis in cancers. In this review, we analyse MYC gene networks in solid cancers. We investigate the interaction of MYC with long non-coding RNAs (lncRNAs). Furthermore, we investigate the role of MYC regulatory networks in inducing changes to cellular processes, including autophagy and mitophagy. Finally, we review the interaction and mutual regulation between MYC and lncRNAs, and autophagic processes and analyse these networks as unexplored areas of targeting and manipulation for therapeutic gain in MYC-driven malignancies.
Highlights
Introduction to MYC Transcription Factors andTheir Roles in CancerThe MYC family of proteins are basic helix-loop-helix leucine zipper transcription factors (TFs) under tight transcriptional regulation
We address the role of MYC as a transforming oncogene in multiple cancers and how MYC is influenced by long non-coding RNAs (lncRNAs) and may be implicated in crucial prosurvival cellular processes such as autophagy
Long Non-Coding RNAs (LncRNAs) have been shown to interact with TFs, including MYC, often via direct regulation of their expression, protein stabilisation, and activity or via indirect regulation of other molecules involved in their expression and activity [32,33,43]
Summary
The MYC family of proteins are basic helix-loop-helix leucine zipper (bHLHZip) transcription factors (TFs) under tight transcriptional regulation. Β-catenin accumulates in the nucleus and, in association with T-cell factor/ lymphoid enhancer factor (TCF/LEF), activates Wnt signalling target genes, including MYC. Alterations to MYC expression and function are found in multiple malignancies, including cancers of the central and peripheral nervous system such as glioblastoma multiforme, and neuroblastoma (NB) [18,19] In many of these cancers, MYC hijacks cellular and molecular programmes through an extensive network of target genes, effectors, regulators, and signalling pathways. This study demonstrated that MYC-mediated transformation sensitised cells to autophagy induction by the linamarase/linamarin/glucose oxidase system (lis/lin/GO), which activated the AMPK pathway and upregulated autophagy genes [34,35,36] These studies revealed a central role for MYC-mediated cellular functions, signalling, and metabolic pathways. We discuss both these aspects of MYC pathology to identify novel therapeutic strategies that may be implemented to effectively establish MYC as a valid candidate for onco-therapy
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